Broadly, our research seeks to define the common elements and differences between the molecular neurocircuitry underlying responses to "natural" reward (i.e. food) versus that which mediates responses to drugs of abuse and the development of addiction. We investigate the regulation and integration of these circuits with the longer term goal of understanding their relevance in both evolution and human disease. It is notable that the motivation to ingest food, though highly adaptive during most of our natural history, has proven to be incompatible with the current state of excess food supply. Understanding the motivational systems that control feeding will give us insight into the molecular mechanisms of a complex behavior, and will ultimately serve to better define the etiology of obesity and eating disorders.
While there have been identified important circulating factors, such as leptin, that convey nutritional and energy supply status to the brain, the mechanism by which this information is processed and integrated within the brain remains a mystery. Our data suggest a number of molecular links that connect traditional "feeding centers", such as the hypothalamus, to "reward centers," such as the mesolimbic dopamine systems.
Our experiments depend upon our ability to effectively manipulate gene function in adult brain neurons. We continue to develop viral and transgenic techniques for conditional genetic analysis of neural function and behavior, including the development of viral constructs that will allow for more systematic studies of gene function in the context of neural circuits.